19. Sepsis is a serious medical condition that is characterized by a whole-body inflammatory state (SIRS) and the presence of a known or suspected infection .
29. Severe Sepsis: Comparative Incidence and Mortality Angus DC, et al. Crit Care Med 2001; American Cancer Society Incidence Cases/100,000 Mortality Deaths/Year
There are over 1 million cases of shock that present to the ED each year. Presentation may be cryptic or obvious. The definition and treatment of shock continue to evolve because of new understanding and technologies. The golden hour represents early intervention.
From 1979 through 1987, gram neg bacteria were the predominant organisms causing sepsis. From 1988 onwards, gram pos bacteria have become the predominant organisms. In 2001, gram (+) bacteria accounted for 52% of cases with gram (-) accounting for 38%, polymicrobial infections 5%, anaerobes 1%, and fungi 5%. ** In 1/3 of cases, no organisms are recovered.
The pathophysiology of sepsis depends on a complex interaction and cooperation between a whole host of cells, including neutrophils, macrophages and structural cells such as endothelial cells, epithelial cells, and dendritic cells. This slide illustrates the response to pathogens, involving “cross-talk” among many immune cells, including macrophages, dendritic cells and CD4 T cells. Macrophages and dendritic cells are activated by the ingestion of bacteria and by stimulation through cytokines secreted by CD4 T cells. These cells secrete a variety of cytokines, chemokines and lipid mediators which can attract further immune cells into the battlefield. The concept has emerged that although initially sepsis may be characterized by increases in inflammatory mediators, as the sepsis persists, there is a shift toward an anti-inflammatory immunosuppressive state. Alternatively, CD4 T cells that have an anti-inflammatory profile (type 2 helper T cells) secrete IL-10, which suppresses macrophage activation. The factors that determine whether CD4 T cells have Th1 (inflammatory) or Th2 (anti-inflammatory) responses are unknown but appear to be influenced by the type of pathogen, size of the bacterial inoculum and the site of infection. Casualties in this battle are the host cells: endothelial cells, epithelial cells in organs such as the lung, kidney and gut and parenchymal cells such as cardiac myocytes. It also has become clear that during sepsis, T cells become anergic or lose their ability to proliferate or secrete cytokines in response to specific antigens. This sepsis-induced anergy seems to be triggered by apoptotic or programmed cell death. Basically, the cells commit “suicide” by the activation of proteases that disassemble the cell. In the case of lymphocytes, a potential mechanism of apoptosis may be stress-induced endogenous release of glucocorticoids.
Sepsis is a common condition. In the US, the incidence of sepsis per 100,000 exceeds AIDS, breast cancer, and first myocardial infarctions. Concerted public awareness campaigns have emphasized the importance of coronary heart disease, AIDS, and breast cancer. Yet, as shown on this slide, the mortality of severe sepsis exceeds AIDS, breast cancer and is only slightly less that that of patients dying suddenly of an acute myocardial infarction. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Incidence, cost and outcomes of severe sepsis in the United States. Crit Care Med 2001; American Heart Association. 2001 Heart and Stroke Statistical Update . Dallas, Tex: American Heart Association, 2000. American Cancer Society. Cancer Statistics . Online edition, accessed 3/29/01.
Severe sepsis shows a small peak in incidence in the very young (<1 year). The incidence then remains low until midlife when it begins to climb. As shown on this slide, both sepsis and severe sepsis are most problematic after the age of 50 years. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Incidence, cost and outcomes of severe sepsis in the United States. Crit Care Med 2001; In Press.
This is an example of moderate pulmonary PBI with a relatively small area of localized pulmonary infiltrates and only slight evidence that the right side was affected. Responders to the scene should be aware that many ballistic vests actually facilitate transmission of the blast wave into an internal stress wave. However, the vest will save the wearer’s life more often than not. This picture shows penetration of fragments around the contour of a vest. Despite (possibly) sustaining a greater degree of pulmonary PBI, the casualty survived because none of the fragments penetrated his mediastinum or thoracic vessels.
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Airway/oxygenation: Mask/intubation Hemodynamic stabilization: Fluid: not unusual for a patient to require 4 to 6 L; stabilization of mentation, BP, respirations, HR, skin perfusion, U.O. > 30 cc/hr Inotropic support: If no response to 3 to 4 L of fluid, start dopamine. If no response with DA at 20 ug/Kg/min, then start NE to keep MAP 60 mm Hg Empiric antimicrobial therapy: Whenever possible, blood, urine, CSF should be sent for gram stain and culture before antibiotics are instituted. Antibiotics should be broad spectrum to cover all potential pathogens. Neonates: Ampicillin + Cefotaxime. Infants: Ampicillin + Cefotaxime or Ceftriaxone Children (> 3 Mos): Cefotaxime or Ceftriaxone. Adults: 3 rd generation Cephlasporin or Antipseudomonal beta lactamase-susceptible PCN +/_AG. If high suspicion of GPC, add Vancomycin or Naf. If GNR, add clinda or flagyl. Bicarbonate: HCO3 for pH < 7.2. Treatment of DIC: 1. Eliminate the underlying disorder or source of infection, 2. Replace components as needed, 3. Arrest intra-vascular clotting process. Steroids: only in patients with suspected or documented adrenal insufficiency.,
MANAGEMENT There are two goals in the treatment of hemorrhagic shock: control of hemorrhage and maintenance of oxygen delivery. The definitive therapy of hemorrhage is control of the source of bleeding; this often requires operative intervention. Thus, for most patients with hemodynamic instability secondary to hemorrhage, prompt surgical consultation and intervention are mandatory. Prehospital Treatment There have been many debates in recent years over the extent to which patients should be resuscitated prior to operative intervention, both in the prehospital setting and the ED. The concept of field stabilization of trauma victims has been discredited for those with hemorrhagic shock. The prehospital interventions that improve survival include attention to the airway, ventilation, immobilization, and rapid transport; not fluid resuscitation. Standard prehospital interventions directed at restoring blood pressure, such as application of a pneumatic antishock garment (PASG) and infusion of intravenous fluids, have not been shown to improve survival.
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